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82 Cards in this Set

  • Front
  • Back
Salivary glands functions (3)
Moistening
Buffer (ductal cells secrete bicarbonate)
Amylase to break starch bonds
Enteric nervous system (myenteric vs submucosal plexi)
Myenteric - between longitudinal and circular muscle layers, control over GI motility
Submucosal - senses lumen environment, regulates blood flow and epithelial cell functions
Gastrin (source, target, action)
Source: Antrum of stomach
Target: Parietal cell in stomach
Action: H+ and pepsinogen secretion
Cholecystokinin (CCK) (source, target, action)
Source: Duodenum and jejunum
Target: Pancreas + gallbladder
Action: Enzyme secretion, contraction
Secretin (source, target, action)
Source: Duodenum
Target: Pancreatic and biliary ducts
Action: Bicarb and fluid secretion
Gastrin-releasing peptide (source, target, action)
Source: Vagal nerve endings
Target: Antrum of stomach
Action: Gastrin release
Somatostatin (source, target, action)
Source: Stomach + duodenum
Target: Stomach, liver, pancreas
Action: Gastrin release, endocrine/exocrine secretions, bile flow
Gastric inhibitory pepitde
Source: Duodenum and jejunum
Target: Pancreas
Action: Decrease fluid absorption
Stomach secretions (5)
H+ -cleaves pepsinogen
Pepsinogens
Mucus
Intrinsic factor (for B12)
Water
Gastric pits
Neck cells rich in mucus secretion
Basal cells: parietal secrete H+, chief (more basal) secrete pepsinogen
How is trypsinogen activated?
Cleaved by enterokinase on enterocyte membranes
Cleaved trypsin is autocatalytic and can also cleave other pro-enzymes/zymogens
What causes contraction of the gallbladder during eating?
CCK
Bile acids (3)
Primary and secondary (eg cholic and deoxycholic)
Amphipathic
Interact w/ cholesterols and phospholipids to form micelles
Regulation of bile secretion (3)
Vagus nerve stimulates liver bile production
Fatty acids and a.a. in chyme stimulate CCK secretion into blood -> gallbladder contraction
Acidic chyme stimulates secretin into blood -> enhances flow of bicarb rich bile from liver
Epithelial cells in lining of small intestine (5)
Absorptive - a.a., glucose, enzymes
Goblet - mucin
Enterocyte - gastrin, cck, secretin
Stem - cell renewal
Paneth - lysozyme
Sugar absorption
Na-coupled transport
Glucose/galactose/fructose
Protein absorption
As small peptides and amino acids by membrane bound peptidases and specific transporters
Fat absorption
Cells take up hydrophobic materials from micelles
Pancreatic lipase -> MAGs -> glycerol and free FAs
Water absorption
9 L pumped into GI tract per day
8 reabsorbed by small intestine
100 mL excreted in feces
Acromegaly and 2 facts about GH
Excess growth hormone AFTER closure of epiphyseal plates
Gigantism results if excess is before
Mediated by IGF-1
GH stimulates lipolysis in adipocytes
What type of hormone are the thyroid hormones?
Amino acid derivatives
Hormone half-lives and degradation
Steroid - long, 1hr, degraded/conjugated in liver
Polypeptides - minutes, RME + lysosomal degradation
Amino acid derivatives - Epi and Norepi in seconds, T3 in days
Types of cell-surface receptors
Ion channel-linked (electrically excitable cells)
G protein-linked
Enzyme-linked (mostly protein kinases)
G protein linked cell-surface receptors (3)
Single polypeptide chain that spans membrane 7 times
Signal is relayed by heterotrimeric GTP binding proteins (G proteins) which are GTPases
Regulate intracellular second messengers (cyclic AMP/GMP, Ca++)
Mechanisms of G protein receptors (4 steps)
Inactive: G protein's α unit is bound to GDP
Ligand binds receptor and GDP is exchanged for GTP
α unit detaches from G protein to interact w/ downstream targets
Life time is short and GTP is quickly hydrolyzed to GDP with reassociation of alpha unit
cyclic AMP (effect, synth)
Activates regulatory subunits of kinases
Synth'd by membrane-bound adenylate cyclase and rapidly destroyed by cAMP phosphodiesterase to 5'-AMP
cAMP activates protein kinase A -> CREB
Calcium ion regulation (2 major pathways)
Cells actively pump out
ER also has a pump to increase Ca concentration in ER
1. Nerve cell depolarization causes influx of Ca
2. Release of Ca from ER via IP3
PIP2 (2 major effects)
G-protein linked receptor initiates phospholipase C hydrolysis of PIP2
-> diacylglycerol (DAG) -> activates protein kinase C
and -> IP3 -> release of Ca from ER
Enzyme-linked receptors (what 3 hormones?)
Usually tyrosine kinases activated upon ligand-binding
Activated by dimerization or conformational change
GH, Insuline, Epo all signal thru tyrosine kinases
What three hormones act through intracellular receptors?
Steroids
Vitamin D
Thyroid hormones
What does cGMP regulate? (2)
Phototransduction
Smooth muscle contraction in response to NO
4 main kidney functions
Filter blood to generate fluid free of cells and proteins
Reabsorb solutes and water from tubular fluid
Secrete other solutes into tubular fluid
Excrete via urine remaining water and solutes
Macula densa
In distal tubule
Senses fluid flow
Signals juxtaglomerular cells in afferent arteriole to produce renin
Juxtaglomerular cells
Produce renin
Help control constriction of afferent and efferent arterioles
How does kidney control body fluid volume vs osmolality?
Body fluid volume by Na excretion
Osmolality by water excretion
Excretion = ?
Filtration - Reabsorption + Secretion
Glomerular filtration rate
20% of plasma is filtered into Bowman's space
125 mL/min
Renal plasma flow and filtration fraction
Renal plasma flow = 650 mL/min
Filtration fraction = 20% = GFR/RPF
Renal clearance
Volume of plasma per unit time from which X has been completely removed and exreted
Cx = Ux * V / Px
U = concentration of x in urine
V = urine flow rate
Px = concentration of x in plasma
Excretion rate
Ux * V
(so clearance = excretion rate / plasma concentration)
Measuring GFR
Using inulin which is freely filtered and not absorbed or secreted
All of inulin is the result of filtration so rate of excretion = rate of filtration
Kidney regulation by norepinephrine (action, released in response to?)
Vasoconstrictor of afferent and efferent arteriole
Released in response to decreased blood pressure or volume
Decreases GFR and RBF
Kidney regulation by nitric oxide (action, released in response to?)
Dilates afferent and efferent arterioles, increasing GFR and RBF
Released by endothelial cells in response to increased intake of NaCl
What is the primary driving force for Na uptake in the nephron?
Na-K ATPase in basolateral membrane of epithelial cells keeps cytoplasmic Na concentration low
Proximal tubule (3 and diabetes mellitus)
Water and Na reabsorption
Isoosmotic: water follows Na passively
Na transport is couple apically to H+ antiport and glucose symport
If Pglucose > 2-3 mg/mL then cotransporters are overhwlemed and glucose appears in urine
Thin descending limb
Highly permeable to water and interstitial fluid has high osmolarity
Thin ascending limb
Impermeable to water but permeable to Na and Cl passively
Thick ascending limb (2)
Na/K/2Cl transporter couples uphill movement of K and Cl to downhill movement of Na -- all 3 ions are reabsorbed
Paracellular cation absorption
Early distal tubule (2)
Impermeable to water
Na/Cl symporter
Late distal tubule and collecting duct (3)
Principle cells reabsorb Na and secrete K
High plasma osmolarity -> ADH secretion -> increased # water absorption channels and vice versa for low osmolarity
Diabetes insipidus
No ADH response so consume lots of water to balance high excretion
What happens if Na intake > Na excretion?
Increased plasma osmolarity
Water form ICF to ECF
Volume expansion
--Volume contraction if intake < excretion
Sympathetic nerve activity (SNA)
Stimulated by volume contraction
Increases renin secretion and Na reabsorption
Decreases GFR
Renin/Angiotensin
Stimulated by decreased afferent arteriole pressure
Renin cleaves angiotensinogen to angiontensin which is cleaved to angiotensin II by ACE
Increases blood pressure and Na reabsorption
Aldosterone
Stimulated by increased angiotensin I + Kplasma
Increases collecting duct Na reabsorption
ADH
Stimulated by increased plasma osmolarity and volume contraction
Increases CD water reabsoprtion
Atrial natriuretic peptide (3)
Stimulated by volume expansion
Increases GFR
Decreases renin, aldo, ADH
Response decreased ECV (volume contraction)
Up: SNA, renin, aldosterone, ADH
Down: ANP, Na/H2O excretion
K+ homeostasis
Small rise in plasma K+
-> aldosterone
-> increases K+ secretion by increasing Na-K ATPase in apical K+ channels in principal cells
Ca++ homeostasis
Only regulated in late distal tube and CD, but taken up in all of nephron
Hypocalcemia -> calcitrol + PTH stimulate Ca absorption in gut and reabsorption in kidney
pH homeostasis in kidney
Alpha intercalated cells of late distal tubule and CD contain ATP-driven proton pump to excrete H+
Also have Cl/HCO3 exchanger to secrete bicarb to interstitial fluid
Leydig cells (stimulated by, secrete, induce)
Stimulated by chorionic gonadotrophin
Secrete testosterone (induces Wolffian duct) + DHT (Induces penis, prostate, urethra)
Sertoli cells
Secrete mullerian inhibiting factor causing regression of mullerian duct
Turner's and Klinefelter's
Turner's - XO, , female phenotype w/ no ovaries/menses/puberty
Klinefelter's - XXY, male but sterile genitalia
Androgen resistance developmental disorder (3)
Male
But can have complete development have normal female genitalia
MIS was produced so lack Muellerian duct
Male puberty tanner stages
I - prepuberty, pre adolescent
II - testicular enlargement, early pubic hair
III - penile enlargement
IV - growth of glans of penis
V - complete adult genitalia
HPA axis basics
Hypothalamus - GnRH
-> Pituitary - LH and FSH
LH -> Leydig cells -> androgens
FSH -> Sertoli cells -> spermatogenesis + inhibin feedbacks to ant. pit.
Androgen potency (4)
DHT > testosterone > androstenedione > DHEA
Stages in female puberty
Thelarche - breast development
Pubarche - development of pubic hair
Menarche - onset of menstruation
HPA axis in females
LH -> theca cells -> androgens/progestins
FSH -> granulosa cells -> estrogens, progestins, inhibins/activins
4 functions of placenta
Hormones: hCG, hCS
Gas transport
Solute transport
Storage functions
Mother’s contribution to materno-placental-fetal unit
Provides LDL as precursor for steroid hormones
Placental contribution to materno-placental-fetal unit (2)
Produces estrogen and progesterone from maternal LDL
Produces pregnenalone for fetal steroid synthesis
Fetal contribution to materno-placental-fetal unit
Synth DHEAS which is transferred back to placenta for estrogen synth
Parturition: prostaglandins (3)
Stimulate uterine contractions
Softening/dilation/thinning of cervix
Used to induce labor
Parturition: oxytocin (3)
Augments labor
Ferguson reflex - distension of cervix
Constricts uterine blood vessels where placenta used to be
Parturition: positive feedback loop (5)
Cervical stretch -> Oxytocin -> Prostaglandins from uterine wall -> uterine contractions -> cervical stretch
Breast changes during pregnancy
Rising estrogen, progesterone, prolactin increase breast water, electrolyte and protein
Lactation: estrogen
Ductal proliferation facilitated by prolactin
Lactation: progesterone
Acinar epithelial differentiation
Facilitated by estrogen
3 hormones necessary for milk production after lactation
Prolactin, oxytocin, cortisol
Neural pathways of lactation stimulation (Oxytocin and prolactin)
Suckling -> afferent to mesencephalon -> releases dopamine inhibition -> allows prolactin synthesis
afferents also directly stimulate oxytocin release